When we consider the enormous number of cells that proliferate in an individual over the course of a lifetime, cancer is a remarkably rare occurrence. Of course, it is the process of tumor suppression that prevents oncogenesis and allows animals with large numbers of cells to survive for years. The two major and general checks on carcinogenesis are the processes of cellular senescence and apoptosis. Although these appear to be fundamentally different in their final outcome, both processes have a number of similarities. The elucidation of nature and mechanisms of these similarities are a major goal of this meeting. Both apoptosis and senescence are irreversible after a point of no return, and function as anti-tumor mechanisms that can be disrupted as part of oncogenesis. Many of the upstream inducers and regulators are common to both, and stressors that trigger apoptosis in one cell type will induce senescence in another. These include telomere malfunction, oncogene activation, and DNA damage. The regulation of senescence and apoptosis is affected by common signaling pathways, including p53, PI3-kinase and AKT, stress-induced kinase pathways, and nuclear factor-kappaB. In addition to roles in checking cancer, or perhaps as a consequence of these roles, apoptosis and senescence contribute to aging. The goal of this meeting is to bring together experts in apoptosis, senescence, and oncogenic transformation in order to explore the similarities and differences in these processes. The interconnections between these biological events and the overlapping principles that emerge represent an emerging field in biology and biomedical research.